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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alloxan diabetes was induced in inbred rats that then were divided into four groups consisting of unoperated diabetic controls, sham-operated diabetic controls, rats given pancreaticoduodenal isografts, and rats given duct-ligated pancreas isografts. The animals were studied for from 18 months (controls) to two years (transplants) and the following important results were obtained: 1) In striking contrast to the diabetic controls, pancreas transplants of both types produced immediate and permanent relief of hyperglycemia, immediate and lasting elevation of serum insulin levels, a normal weight and growth curve, and good health for two years. Removal of the graft was followed by recurrence of severe diabetes. 2) Pancreas transplants of both types prevented the widespread and severe renal, ophthalmic and neural lesions of diabetes that were found in the diabetic controls. 3) The duct-ligated pancreas graft and pancreaticoduodenal transplant were equally effective in controlling diabetes. Ligation of the pancreatic duct was not followed by significant morphologic or clinical evidence of pancreatitis or by loss of endocrine function. 4) Portal venous drainage of the pancreas transplant was unnecessary for good endocrine function.
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PMID:Long term studies of pancreas transplantation in experimental diabetes mellitus. 109 93

To elucidate the hemodynamic changes in the course of acute pancreatitis in dogs, various parameters were monitored non-invasively and real-timely by the ultrasonic flow probes which had been placed in advance. The dogs were divided into two groups, i.e., control group (CG) and infusion group (IG). In the infusion group, lactated Ringer solution was infused intravenously for 12 hours in order to maintain LAP or CVP at the mean +/- 1 mmHg of its control value before inducing pancreatitis. In the control group, lactated Ringer solution was not infused. Cardiac output (CO) and LV dp/dt abruptly decreased in a few hours and remained low levels in a control group (CG), but not in an infusion group (IG). It shows that the decreased CO was caused by a decrease in preload but not by a depression of contractility. Gastroduodenal arterial flow (GDAF) and GDAF/CO decreased in a few hours and kept low level in CG, but not in IG. Therefore, a decrease in GDAF is mainly caused by an increase in vascular resistance due to an increase in Hematocrit. Superior pancreatico-duodenal venous flow (SPDVF) and SPDVF/CO decreased immediately in both groups, revealing that there is severely depressive outflow from pancreas because of hemorrhage and destruction of pancreatic parenchyma immediately after the onset of pancreatitis. In CG, Total hepatic flow (THF) and Portal vein flow (PVF) gradually decreased in a few hours and kept low levels, but Common hepatic arterial flow (CHAF) did not decrease. This suggests that decrease of THF is due to decrease of PVF. THF/CO increased in CG. PVF/CO decreased in CG, while CHAF/CO increased in both groups. The increased CHAF compensated for the decreased PVF, which may play an important role in protecting the liver.
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PMID:Non invasive analysis of hemodynamic changes in dogs with acute pancreatitis. 172 93

Splenopancreatic disconnection (SPD) was conceived and implemented as a technical addition to distal splenorenal shunt (DSRS) to maintain its selectivity and preserve portal perfusion. The proposed hemodynamic and metabolic stability of hepatocytes after DSRS-SPD should improve survival. In this nonrandomized study, 145 consecutive (Child A/B) variceal bleeders were electively subjected to selective shunt with DSRS in 93 and DSRS-SPD in 52 patients. The 2 groups were similar before surgery with a mean follow up of 24 +/- 12 (DSRS) and 27 +/- 14 (DSRS-SPD) months. DSRS-SPD had an operative mortality of 3.8%. Postoperative pancreatitis occurred in 7.7% after DSRS-SPD and 3.2% after DSRS alone, with schistosomal hepatic fibrosis representing 86% of morbid cases. Shunt patency was high and recurrent variceal hemorrhage was low in both groups. Clinical encephalopathy was significantly reduced after DSRS-SPD (p less than 0.05). The addition of SPD significantly reduced both the incidence of chronic hyperbilirubinemia in the schistosomal patients (p less than 0.05) and the difference between the changes in total serum bilirubin in all patients (p = 0.001). Portal perfusion was preserved after DSRS-SPD in all of the angiographically-studied patients. The overall survival was 84% after DSRS and 88% after DSRS-SPD. The schistosomal patients showed an incidence of 95% and 96% survival after DSRS and DSRS-SPD, respectively. DSRS-SPD was able to improve survival (92%) better than DSRS (77%) among well-matched nonschistosomal patients. These data show: (1) DSRS-SPD still has low operative mortality and a high patency rate with a low incidence of recurrent variceal hemorrhage, (2) DSRS-SPD maintains portal perfusion, achieves better survival, and reduces the incidence of encephalopathy, especially in patients with nonalcoholic cirrhosis and mixed liver disease, (3) in the schistosomal population, DSRS-SPD reduces the incidence of chronic hyperbilirubinemia but increases the risk of postoperative pancreatitis.
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PMID:Should both schistosomal and nonschistosomal variceal bleeders be disconnected? 185 19

Portal and splenic venous thrombosis is a rare but well recognised complication of pancreatic carcinoma and pancreatitis. We report a series of five patients with pancreatic disease in whom CT detected this complication. The appearances on CT are of an enlarged vein with a centre of lower attenuation which does not enhance following intravenous contrast injection, ring enhancement and opacification of collateral veins. Splenic vein thrombosis following pancreatitis should be considered in all patients with pancreatic disease as this complication is increasingly recognised as a cause of upper gastrointestinal haemorrhage from varices.
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PMID:Splenic and portal venous thrombosis: a vascular complication of pancreatic disease demonstrated on computed tomography. 229 61

Somatostatin is an inhibitory hormone that decreases the secretion and end organ response of cholecystokinin (CCK). Inhibition of hormonal stimulation of pancreatic exocrine secretion by somatostatin may improve the course of acute pancreatitis. Anesthetized dogs underwent cholecystectomy and cannulation of the pancreatic duct, thoracic duct, and portal vein. Twenty experiments were performed in random order with 5 dogs in each group. Hourly measurements of lymph flow and portal and thoracic duct amylase were made. Portal blood insulin, glucagon, and CCK concentrations were determined by radioimmunoassay on samples obtained at the beginning and end of the experiments. Pancreatitis was induced by injecting, under constant pressure, 10 ml bile into the pancreatic duct during 1 min. Somatostatin was administered intravenously (20 micrograms/kg/hr). After 5 h, the dogs were killed, pancreas glands removed and weighed and tissue samples obtained for histologic evaluation. There was a significant increase in lymph amylase output and portal venous amylase and CCK concentrations in the dogs with pancreatitis compared to the control dogs. In dogs with pancreatitis, lymphatic amylase secretion and portal CCK concentrations were significantly decreased by somatostatin. Somatostatin did not significantly alter portal amylase concentrations, pancreas gland weights or histologic inflammation when compared to values from dogs with pancreatitis not treated with somatostatin.
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PMID:Effects of somatostatin on acute canine experimental pancreatitis. 244 77

We investigated the effects of hypercalcemia on pancreatic duct permeability and pancreatitis in cats. Acute hypercalcemia was maintained by an infusion of calcium gluconate; controls received saline solution. Chronic hypercalcemia was maintained by diet and by vitamin D and dihydrotachysterol injections. Portal venous blood was analyzed for large dextran molecules that had been perfused through the pancreatic duct. In a separate group of hypercalcemic animals, we perfused the duct with activated pancreatic enzymes to induce acute pancreatitis. After 24 hours of hypercalcemia, dextrans were detected in the portal venous blood of 6 of 11 hypercalcemic and none of the 6 control animals (p less than 0.05). After 12 hours of hypercalcemia, dextrans were detected in all 7 hypercalcemic and 1 of 7 control animals (p less than 0.001). The degree of pancreatic inflammation was greater in the 12-hour animals than in the controls (p less than 0.001). After 14 days of hypercalcemia, however, there were no differences in dextran permeability or pancreatitis in experimental or control animals. Our results indicate that acute hypercalcemia increases the permeability of the pancreatic duct to molecules the size of pancreatic enzymes. This could be important in the pathogenesis of acute pancreatitis associated with hypercalcemic states.
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PMID:Acute hypercalcemia, pancreatic duct permeability, and pancreatitis in cats. 245 25

1. We have assessed the role of platelet-activating factor in caerulein-induced acute pancreatitis (four subcutaneous injections of caerulein at a dose of 20 micrograms/kg) by measuring platelet-activating factor levels in portal blood, pancreatic tissue and peritoneal exudate in rats with and without pancreatitis. 2. We have also observed the effect of the platelet-activating factor antagonist, BN-52021, on the hyperamylasaemia and exocrine pancreatic secretion impairment associated with pancreatitis. 3. In rats with pancreatitis the basal pancreatic flow rate was increased (1.63 +/- 0.41 versus 0.25 +/- 0.03 microliters/min). Total protein output was similar in both untreated (5.98 +/- 1.93 micrograms/min) and caerulein-injected (6.5 +/- 2.0 micrograms/min) animals. Amylase output was lower in rats with pancreatitis (19.6 +/- 4.8 mu-units/min) than in controls (39.4 +/- 16.6 mu-units/min). 4. Caerulein-treated animals had significantly higher serum amylase levels than untreated animals. BN-52021 significantly reduced the caerulein-induced hyperamylasaemia. 5. Portal blood platelet-activating factor levels increased in rats with pancreatitis and in rats infused with cholecystokinin. Rats injected with caerulein and BN-52021 had portal blood levels of platelet-activating factor that were lower than those with pancreatitis. 6. Morphological derangements associated with pancreatitis (inflammatory infiltration and cell vacuolization) were also markedly reduced in BN-52021-treated animals. 7. The results of this study suggest that platelet-activating factor is involved in the development of caerulein-induced acute pancreatitis in rats.
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PMID:Platelet-activating factor mediates pancreatic function derangement in caerulein-induced pancreatitis in rats. 752 Mar 81

A woman aged 62 with long history of chronic relapsing pancreatitis presented with swelling and ulcer in the lower limbs and occasional gastrointestinal bleeding. The radiological imaging showed complete obstruction of Inferior Vena Cava (IVC) at the level of the pancreas and well developed collateral vessels. Portal vein and splenic vein were also obstructed and superior mesenteric venous blood drained into the liver via coronary vein. She was originally found to have pancreas head tumor, which was not resectable. A palliative operation was performed, but histological examination of pancreatic specimen suggested only chronic inflammation and no evidence of malignancy. She was diagnosed as tumor-forming type chronic pancreatitis. Although SPV or SMV-PV obstruction has been recognized as a complication of chronic pancreatitis, IVC obstruction can occur by the same mechanism. This is the only case but one ever reported. Not only splenoportography but IVC-graphy will contribute to more precise understanding of patient's condition with chronic pancreatitis.
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PMID:Complete obstruction of the inferior vena cava due to chronic relapsing pancreatitis: a case report. 757 86

To study the role of pancreatic blood flow and vasoactive substances in the development of acute pancreatitis, we measured portal vein blood levels of bradykinin, prostaglandin E2 (PGE2), histamine, serotonin, and pancreatic enzymes, and with an electromagnetic blood flowmeter we recorded gastroduodenal arterial flow (GDAF), superior mesenteric arterial flow (SMAF), and mean arterial blood pressure for 6 hr in dogs with acute hemorrhagic necrotizing pancreatitis induced by the retrograde injection of autologous bile (0.5 ml/kg) into the pancreatic duct. GDAF and SMAF decreased immediately in the early phase of acute pancreatitis (-17.8 +/- 6.1%** at 10 min and -15.8 +/- 7.1%* at 20 min; *P < 0.05, **P < 0.01); portal bradykinin concentration increased quickly (3.2 +/- 1.2 pM at 0 time, 16.2 +/- 5.2 pM* at 5 min, 30.4 +/- 4.8** pM** at 10 min, and 39.6 +/- 15.1 pM* at 20 min). Portal PGE2 concentration increased gradually after the induction of acute pancreatitis, and differences from the control group were significant at 20, 30, and 180 min (1426 +/- 175 pM at 0 time, 1956 +/- 273 pM* at 20 min, 2148 +/- 265 pM** at 30 min, and 3369 +/- 686 pM* at 180 min). Portal histamine and serotonin concentrations increased somewhat, but not significantly. These findings suggest that the injection of bile into the pancreatic duct causes the pancreas to quickly release a large amount of bradykinin into the portal vein, which immediately reduces the pancreatic blood flow in the early phase, thus accelerating the progress of acute pancreatitis.
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PMID:Role of pancreatic blood flow and vasoactive substances in the development of canine acute pancreatitis. 769 98

Portal venous thrombosis (PVT) is a condition associated with high morbidity. The etiologies of PVT include intra-abdominal inflammation or infection, surgical intervention, abdominal malignancies such as hepatocellular carcinoma (HCC) and pancreatic carcinoma, or abnormality in coagulation caused by various reasons such as liver cirrhosis. Management of PVT should be based on its etiology and the condition of the patient. We describe a cirrhotic patient with HCC who suffered from acute pancreatitis. PVT in the main trunk was detected at admission due to the episode of acute pancreatitis. The etiology of thrombosis was considered to be inflammation around the main portal trunk caused by pancreatitis rather than cirrhosis or HCC. We did not instigate any management for the thrombosis. Acute pancreatitis was relieved after conservative treatment. Follow-up imaging study performed 46 days after detection of thrombosis showed spontaneous complete resolution of the thrombus. Our experience may provide useful information for the management of such patients.
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PMID:Acute pancreatitis complicated with transient portal venous thrombosis in one patient with hepatocellular carcinoma and cirrhosis. 1752 8


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